This is a review of data on the impact of COVID-19 on blood clotting. An important feature of the pathogenesis of severe acute respiratory syndrome caused by the SARS-Co-2 coronavirus is the risk of thrombotic complications including microvascular thrombosis, venous thromboembolism, and stroke. These thrombotic complications, like thrombocytopenia, are markers of the severe form of COVID-19 and are associated with multiple organ failure and increased mortality. One of the central mechanisms of this pathology is dysregulation of the adhesive protein P-selectin. The study of the mechanisms of changes in hemostasis and vascular pathology, and the role in these processes of biomarkers of thrombogenesis, and primarily of P-selectin of various origins (platelets, endothelial cells, and plasma), can bring some clarity to the understanding of the pathogenesis and therapy of COVID-19.